Burns due to skin contact with flame, hot surfaces, hot liquids etc. are among the three most common accidents, both at the workplace and at home. The effective treatment of burn injuries continues to be a significant concern in the medical field. In North America, it is estimated that about 95% of all burn injuries are treated by home remedies, 2.5 million subjects seek medical advice for burns annually in the US., with about 100,000 of these requiring hospitalization [W. F., Am. Physician, :1321, 1992].
European figures are similar, with about 5% of burn injuries that come to medical attention admitted to hospital and a mortality rate of 0.2% [Jonsson Gynaecol :168, 1980; Hytonen Gynaecol : 218, 1987; de, Burns, :58, 1994]. Most of the burn injuries occur at home, and are essentially scalding accidents with gender and age distributions varying widely by region, urbanization and education. These figures do not include sunburn injury.
The psycho-social impact of burn injuries is dramatic. Over 95% of the costs are incurred by severe injuries, mostly (˜two thirds) in terms of lost working days and to a lesser extent for direct care [de, Ann. Acad. Med. Singapore, :680, 1994; Hansbrough, J. Burn Care Rehabil :377, 1995]. There are, however, essentially no published data that analyze the epidemiology and impact of burn injuries which do not reach medical attention, but which often do cause loss of working days and considerable, if transient reductions in quality of life [Miller, . Physician, :167, 1977; Mertens . North Am., :343, 1997].
The main immediate burn injury problems include pain and primary infection. Scarring and functional impairment characterize the intermediate term. Malignancy represents a long term risk, although this is rare for most burns except those from ultraviolet and other radiation. Beyond the well known misery of burn pains, the objective threats, severity and prognosis of burn injuries are all functions of injury extent, i.e. surface area and depth of tissue destruction. The total tissue destruction is the sum of cells directly destroyed by heat and the much larger number of cells dying due to local tissue responses including edema, leukocytic infiltration, local mediators, apoptosis and primary infection. These elements are fundamental and similar in small as well as massive burn injuries, the latter adding systemic responses in a critical care scenario with mortality rates increasing as a quantitative function of tissue loss, infection and post-burn immunosuppression.
The principles of burn therapy have changed little over the past decades, and there is some lack of basic science and animal models for in depth analysis of the cellular and molecular events following tissue burn injury. There is long-standing consensus for rapid and aggressive intervention following burn injury, including the early use of skin grafting. One conclusion from this recognized need for rapid intervention is that following the direct tissue destruction by the hyperthermal insult, it is local and systemic biological responses that determine much of the post-injury course.
This scenario is analogous to, and may include, the development of shock syndromes which can be by themselves life threatening, independently of the nature and extent of a given injury [Cason, Pediatr . Surg.,:3, 1981]. Other than shock, however, the immediate interference with tissue injury responses following thermotrauma has received little attention beyond general pain relief and precaution against infection [Baxter, C. R. and Waeckerle :1305, 1988; Brofeldt, J. Burn Care Rehabil., :63, 1989]. Secondary cell death due to tissue burn injury responses involves the elements of acute phase reactants such as leukocyte extravasation and mediator release. Vasoconstriction occurs peripheral to the injury locus but hyperemia and fluid loss within the injured area conspire to reduce oxygenation, accumulate toxic detritus, and activate complement and apoptosis pathways for pronounced secondary cell death. These events create the vicious circle characteristic of even small burn injuries and their misery [Shaw, A, Br. J. Hosp. Med., :583, 1994; Arturson, G., Burns,: 255, 1996].
In addition, the injured tissue represents an ideal, immunologically underprivileged target site for infectious agents which can dramatically threaten the recovery process. While the need to cover burn injuries has long been recognized, ideal solutions are still elusive, and the variety of proposed remedies is profuse, ranging from honey, tree bark and animal urine or dung to potato peels to amniotic membranes, allografts and modern plastics to name but a few.
The use of tannic acids (TA) (or tannic herb extracts) as a burn remedy had been proposed early this century [Davidson, E. C., Surg. Gynecol. Obstet., 1925] based upon ancient Chinese texts. TA is the collective name for a group of undefined substances which convert putrefiable hide or skin into imputrescible leather. TA occurs in most parts of the vegetable kingdom and is more prevalent among the higher plants, especially in the barks of trees (cited from: Hupkens, Burns,:57, 1995). The acidity of these extracts is uncertain, as hydroxy groups from the trihydroxybenzene structure are extremely weak proton donors. The often ill described tannic herb extracts differed in their hepatotoxicity and tendency towards secondary infection [Hupkens, 1995]. TA treatment has been linked to liver necrosis in burn patients and even death: in one report 14 of 16 TA-treated patients who died from their burn trauma showed definitive evidence of serious liver necrosis (reviewed in [Hupkens, 1995]). This level of toxicity is unacceptable and has lead to the disappearance of TA from medical practice, although the burn toxins (a 70 year old concept no longer acceptable) released in the wound and relied on TAs ability to absorb/precipitate these putative toxins.
The use of vinegar as an antimicrobial agent is as old as the use of alcohol, and by around 1000 AD, hand washing with vinegar was recommended in ancient medical texts from China and Arabic sources such as (1031–1095 AD) [Chan, Nephrol: 295, 1994].
Vinegar is an impure organic acid and a rich source of many volatile contaminants [De, Food Add. Contam 161, 1987]. It has possible antibacterial and antiviral effects, although the mechanisms of this vinegar activity is unknown. Vinegar is approved for human non-dietary use and performs well as the main ingredient of vaginal douches although mechanisms are, again, uncertain [Brinton Gynecol :49, 1990; Nyirjesy, Obstet. Gynecol :50, 1997]. The effectiveness of pure acetic acid, sodium acetate and vinegar have rarely been compared [Brighenti:242, 1995], and never with respect to antimicrobial activity. Although sodium acetate is used in some vaginal douches, their effectiveness has not been measured [Chvapil, Obstet. Gynecol :88, 1978]. While acid sensitivity of bacteria is one element of antimicrobial activity, this is insufficient to explain the antimicrobial effects of vinegar, since some common food-borne bacteria are highly sensitive to vinegar, yet they survive gastric acid exposure and cause common intestinal disease [Nishikawa, Int. J. Food Microbiol., :271, 1993]. There is a considerable amount of published literature on the antimicrobial effects of vinegar [Larghi. Argent. Microbiol :86, 1975; Fasanella, Ophthalmic. Surg., 1991; Karapinar, S. A., Int. J. Food Microbiol :261, 1992; Nishikawa Ostomy. Wound Manage., :18, 1996], observations that are finding their way into the food processing industries [Dickens :576, 1994; Entani Kansenshogaku Zasshi :443, 1997]. While vinegar treatment of killed chicken prior to freezing was shown to significantly reduce bacterial contamination, there are no published reports on the effects of vinegar on living skin [Dickens, 1994]. A widely employed skin application of vinegar occurs in the Pacific Rim Countries where, acting as a nematocyst inhibitor, vinegar is the recommended first aid treatment against potentially life threatening jelly fish stings [Fenner, Med. J. Aust., :550, 1985; Beadnell Med. J. Aust., :655, 1992; Fenner, Med. J. Aust., :498, 1993]. In vitro tissue culture studies suggested that acetic acid is toxic to human fibroblasts and keratinocytes in concentrations of above 0.025% (reviewed in [, C. R., 1996]). These data contrast with the frequent use of vinegar douches, which are tolerated well and over prolonged periods of intravaginal use [Nyirjesy, Obstet. Gynecol:50, 1997].